Most U.S. campaigns to increase public awareness about the health effects of alcohol consumption have focused on underage drinking, binge drinking, or drinking and driving (37–39). Studies conducted in other countries suggest potential efficacy of communication strategies to increase cancer-relevant awareness. For example, a Canadian container label intervention demonstrated a 10% greater increase in knowledge of alcohol as a carcinogen in the intervention vs. the comparison group two months post-intervention (40). Another study found that using multiple and diverse information sources can reduce alcohol use intentions as compared to reliance on a single source (41). A high proportion of American adults, both drinkers and non-drinkers (35), are unaware of the association between alcohol consumption and cancer risk.
Hospitals, labs, and health departments try to cope with blood culture bottle shortage
However, when results from a study were published in a single paper but also within a pooled analysis that included other unpublished results, we chose the pooled analysis, even if the individual study provided the most detailed or recent information. (3) Studies that reported standard errors or confidence intervals (CIs) of the risk estimates or provided sufficient data to calculate them. Since women rarely drink alcohol in China, the main analysis focused on men, a third of whom drank regularly (most weeks in the past year).
3. Retinoic Acid Metabolism
- In summary, several reports indicate that alcohol consumption decreases survival of patients with cancer, whereas other studies did not observe this association.
- Numerous epidemiological studies have consistently demonstrated a dose-response relationship between chronic alcohol consumption and increase in the risk for breast cancer [21,22].
- And not only do women usually experience the immediate effects of alcohol more quickly than men, but they are also at a higher risk for alcohol’s long-term health effects.
- But the All of Us study, Dr. Cao and her colleagues explained, offered a unique opportunity to take a robust look at people in these groups in the United States.
Retinoid metabolism and the normal function of the immune system are both impaired by ethanol, while ethanol may lead to increases in sex hormone levels, as well as dysbiosis of the microbiome and liver cirrhosis. “For some risk factors, the exposure is generally more common or intense in some organs, for example, tobacco smoke in [the] lung, and this may play a role in a stronger association between smoking and lung cancer,” Islami explained. When they further analyzed their data incorporating former drinkers and including the two cancers possibly linked to alcohol, the numbers went up significantly. “When we did the analysis and included former drinking, pancreatic and stomach cancers, the numbers increased to 925,000 alcohol-related cancers,” she said.
What is the evidence that alcohol drinking can cause cancer?
Alcohol research and control efforts supported by multiple governmental and non-governmental organizations (NGOs) internationally have found that the public health impact of harmful alcohol consumption is substantial. In 2016, it resulted in an estimated 5.1% of the global burden of disease and injury, and 5.3% of deaths (1). A large meta-analysis of 23 health outcomes showed that the number of daily alcohol beverages that minimized harm overall was 0 (95% uncertainty interval 0.00–0.08) (2). In the study, many people being treated for cancer and longer-term cancer survivors reported regularly drinking alcohol—many moderately, but some also heavily and often. According to the study’s findings, male long-term survivors and younger people being treated for cancer were among those who were particularly likely to be heavy or frequent drinkers. Study lead author Farhad Islami also noted that “there is accumulating evidence” that alcohol can cause other types of cancer like pancreatic cancer.
Researchers also studied the effects of alcohol on estrogen receptor–negative mouse mammary tumors. One study involving estrogen receptor–negative Met-1 cancer cells used female FVB/N mice that consumed 20 percent w/v ethanol in drinking water for 18 weeks before they were injected subcutaneously with the cancer cells (Hong et al. 2010). Compared with water-drinking control mice, the ethanol-drinking animals developed palpable tumors earlier and also developed larger tumors. Several other parameters (i.e., insulin sensitivity, leptin levels in the blood, and estrogen levels) were elevated in the alcohol-consuming mice.
Alcohol Consumption and the Risk of Cancer
The genotoxic drug diethylnitrosamine (DEN) has been widely used to induce hepatic carcinoma in rodents [97], and is the most commonly used chemical to induce liver cancer in mice. The co-treatment of mice with DEN and CCl4 resulted in dramatic increase in the liver tumor incidence where 100% of the animals in the co-treatment group developed liver tumors [98]. Recent studies show that combination of DEN followed by alcohol exposure increase incidence of HCC promoted by underlying alcoholic liver disease [99]. Experimental model of chemically induced HCC in male BALB/c mice https://rehabliving.net/ was developed in which DEN initiation with CCl4 and ethanol promotion induced a two-stage liver carcinogenesis mimicking the usual sequence of events observed in human HCC [100]. However, some individuals with the defective form of ALDH2 can become tolerant to the unpleasant effects of acetaldehyde and consume large amounts of alcohol. Epidemiologic studies have shown that such individuals have a higher risk of alcohol-related esophageal cancer, as well as of head and neck cancers, than individuals with the fully active enzyme who drink comparable amounts of alcohol (31).
More than half of teenagers aged 15 to 17 surveyed for the research found zero alcohol drink packaging attractive. The Australian Cancer Council has raised alarm bells about zero-alcohol drinks following research into their impact on teenagers. “It’s a risk that you face every day, and that also means that the reduction of the risks can benefit you every day as well.” A previous headline for this story on the NPR homepage incorrectly said 34 million cancer cases had been linked to alcohol use in 2020.
Noelle LoConte, M.D., an oncologist at the University of Wisconsin-Madison who studies alcohol and cancer risk, said that these findings confirm what doctors have long observed. Because cancer is a relatively rare outcome, we assumed that ORs, risk ratios and rate ratios were all comparable estimates of the RR. Measures of association and the corresponding CIs were translated into log(RR)s and their variances (Greenland, 1987). We performed a literature search in MEDLINE, ISI Web of Science (Science Citation Index Expanded) and EMBASE for epidemiological studies published online before September 2012. For the sake of completeness, we also reviewed references from all relevant studies, reviews and meta-analyses published on the alcohol–cancer association to identify additional studies. To date, numerous studies have demonstrated genetic modeling as a promising technique for developing tumor models.
Although many factors influence tumor growth and progression, evidence that highlights the role of host immune cells in controlling cancer growth and progression is accumulating. Once some cells are transformed into cancer cells, tumor immune surveillance, also known as tumor immunoediting, comes into play [130]. Alcohol consumption is a well-established risk factor for cancer and has been linked to cancers of the oral cavity and pharynx, oesophagus, liver, colorectum and breast.
Alcohol-induced chronic inflammation in breast adipose tissue creates microenvironment that is conducive to increased tumor cell proliferation, metastasis, and enhanced tumor-related angiogenesis. Increased oxidative stress and continuous secretion of pro-inflammatory cytokines by inflamed adipocytes can elicit epigenetic changes in pre-cancerous cells [55]. It is plausible that inflamed tissue microenvironment offers an ideal setting for tumor onset and progression, and alcohol acts as a major driving force. For cancer specifically, an estimated 4.1% of all new cases globally in 2020 (3), and from 2013 through 2016, 4.8% of all cases annually in the U.S., were attributable to alcohol consumption (4). Current evidence suggests that “[t]here is no threshold of alcohol consumption below which cancer risk does not increase, at least for some cancers ” (5), and cancer prevention guidelines indicate that it is best not to drink alcohol (5, 6).
Further understanding of the carcinogenic properties of alcohol and its metabolites will inform future research, but there is already a need for comprehensive alcohol control and cancer prevention strategies to reduce the burden of cancer attributable to alcohol. The effects of chronic alcohol consumption on tumor growth and metastasis of the highly invasive and spontaneously metastatic B16BL6 melanoma inoculated subcutaneously were studied in female C57BL/6 mice administered ethanol in drinking water. In an initial study, consumption of 2.5 percent, 10 percent, or 20 percent w/v ethanol in drinking water for 6 to 8 weeks before tumor inoculation and continuing thereafter did not affect primary tumor growth (Blank and Meadows 1996).
All of them — including beer, wine and liquor — have ethanol, which is linked to increased cancer risk,” Bevers says. About 5.5% of all new cancer diagnoses and 5.8% of all deaths from cancer are attributed to drinking alcohol, according to the National Institutes of Health (NIH). Because cancer risk increases with the amount of ethanol consumed, all alcoholic beverages pose a risk. The study confirmed that most American adults aren’t aware of the link between alcohol consumption and cancer. It also found that, even among those who are aware, there’s a belief that it varies by the type of alcohol. For example, more participants were aware of the cancer risks from hard liquor and beer than about the risk from wine, with some participants believing wine lowers your cancer risk.
With alcohol consumption rising, particularly in rapidly developing countries such as China, there is an urgent need to understand how alcohol affects disease risks in different populations. Alcoholic beverage production, distribution, and consumption have been regulated throughout the world for centuries (53). However, the federal government retained power to regulate alcohol through control of foreign and inter-state commerce, federal taxes, federal property, and financial incentives. Interpersonal influences, including interactions with family and friends, also shape knowledge and behaviors (42, 43). Because overt behaviors appear to be more susceptible to normative influence than clandestine behaviors (44), alcohol consumption behaviors in groups might be especially subject to social sanction. Increased awareness of the alcohol-cancer link might encourage some people to warn family and friends about consumption, although the efficacy of such communication on behavior is unclear.
Despite substantial epidemiological and mechanistic evidence on alcohol and cancer, several knowledge gaps remain that if filled could improve estimates of the burden of alcohol-attributable cancers, and inform tailord interventions to reduce consumption. Given the study’s findings, “there’s also a need to better understand why so many cancer survivors have such high alcohol consumption,” she continued. Binge drinking was most common among men, people under the age of 50, and former and current smokers. Among those who drank, binge and hazardous drinking was also much more common in those diagnosed and treated for cancer before the age of 18. The fact that drinking alcohol can cause cancer has received increasing attention in the past few years. But the potential threat it poses to people with cancer and longer-term survivors has largely been overlooked, explained Tanya Agurs-Collins, Ph.D., of the Behavioral Research Program in NCI’s Division of Cancer Control and Population Sciences.
The study also found that people who believed drinking alcohol increased the risk of heart disease were more aware of the alcohol–cancer risk than those who were unsure or believed drinking lowered the effect on heart risk. The innate immune response rapidly identifies cancerous and/or precancerous cells and destroys them. This response is recognized by inflammatory mediators (chemokines and cytokines) https://rehabliving.net/40-tips-for-staying-sober-under-pressure/ produced by an array of immune cells, such as natural killer (NK) cells, macrophages, neutrophils, and dendritic cells (DCs) [7]. Upon activation, NK cells produce cytokines and chemokines that generate inflammatory responses and activate adaptive immune response. Macrophages and neutrophils possess both anti-tumor activity as well as immune suppressive activity against tumor cells.
The nearly 4,000 people who took part in the survey were asked how much does drinking several types of alcohol (wine, beer, and liquor) affect the risk of getting cancer. We excluded studies reporting on a specific type of alcoholic beverage only (e.g., beer only) because in those studies the nondrinkers of a specific beverage could possibly be drinkers of other types of alcoholic beverages. Alcohol is a risk factor for cancer of the oral cavity, pharynx, oesophagus, colorectum, liver, larynx and female breast, whereas its impact on other cancers remains controversial.
Previously, the B16BL6 melanoma model established an association between alcohol intake and increased iNKT cell number [156,157,158]. With increasing tumor growth, the crosstalk between alcohol and tumor cells leads to iNKT cell anergy. Therefore, development of immunotherapeutic strategies inhibiting iNKT cell anergy through blocking the interaction between alcohol and tumor cells could emerge as a plausible therapeutic outcome in alcoholics. Myeloid-derived suppressor cells (MDSC) and iNKT cells are key inhibitory cells that modulate CD8+ T cell function in mouse model of alcohol-induced tumors.
